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. 2021 Mar 17;12(4):282. doi: 10.1038/s41419-021-03556-4

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A Co-IP assay showed that LSD1 formed a stable complex with wild-type p53 in SiHa cells. B LSD1 knockdown contributes to upregulation of p53 mRNA and protein expression in SiHa cells (n = 3 per group). C There was a positive correlation between miR-34a and p53 mRNA in cervical cancer according to the normalized counts RNA-sequencing data from TCGA-CESC. D p53 silencing led to downregulation of miR-34a expression in SiHa cells (n = 3 per group). E Nutlin-3a and doxorubicin were used to stimulate p53 in SiHa cells and contributed to upregulation of miR-34a expression in a dose-dependent manner (n = 3 per group). Each experiment was repeated three times. **p < 0.01; ***p < 0.001; ****p < 0.0001.